Crazy Is As Crazy Does

An article in The Atlantic describes fascinating research into the effects of Toxoplasma gondii infection, but what role do domestic cats really play?

Although we’re not even halfway through February, an article in the March issue of The Atlantic is already getting a lot of attention. But with a title like “How Your Cat Is Making You Crazy,” that’s no surprise. (Don’t get me wrong: the article is a great read.)

What is surprising is that the story hasn’t been picked up by the American Bird Conservancy or, more likely, The Wildlife Society.

Not yet, anyhow. Surely, it’s only a matter of days before ABC, TWS, and others (mis)use the article to stir up their witch-hunt against free-roaming cats. A careful read, however, suggests such a move would be both premature and misguided (as if that makes any difference).

But if Flegr is right, the ‘latent’ parasite may be quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents. And that’s not all. He also believes that the organism contributes to car crashes, suicides, and mental disorders such as schizophrenia.

As I say, it’s just a matter of time—and not much of it, I suspect—before TNR opponents jump all over this, shaping it to fit their (tired) message.

I expect to see the lengthy quote from Joanne Webster, a parasitologist at Imperial College London, parsed very carefully, for example. Webster and her colleagues discovered that Toxo-infected rats are actually attracted to cat urine, a phenomenon they dubbed “fatal feline attraction.” Commenting on Flegr’s research, Webster is, in McAuliffe’s words, “more circumspect, if not downright troubled.”

I don’t want to cause any panic. In the vast majority of people, there will be no ill effects, and those who are affected will mostly demonstrate subtle shifts of behavior. But in a small number of cases, [Toxo infection] may be linked to schizophrenia and other disturbances associated with altered dopamine levels—for example, obsessive-compulsive disorder, attention-deficit hyperactivity disorder, and mood disorders. The rat may live two or three years, while humans can be infected for many decades, which is why we may be seeing these severe side effects in people. We should be cautious of dismissing such a prevalent parasite.

…I’m not too worried, in that the effects on humans are not gigantic. If you want to reduce serious car accidents, and you had to choose between curing people of Toxo infections versus getting people not to drive drunk or while texting, go for the latter in terms of impact.

Infection in Humans
“Humans,” explains McAuliffe, “are exposed not only by coming into contact with litter boxes, but also, he found, by drinking water contaminated with cat feces, eating unwashed vegetables, or, especially in Europe, by consuming raw or undercooked meat. According to the Centers for Disease Control and Prevention, the infection rate in the U.S. among those 12 and older is estimated to be 22.5 percent.

And while Toxoplasmosis “can come from cats,” the CDC points out that “people are more likely to get it from eating raw meat or from gardening.”

Nowhere in McAuliffe’s article does she mention the proportion of people infected through contact with cat feces, as compared to those infected from eating raw or undercooked meat. For the purposes of Flegr’s work, the source is largely immaterial. (And, virtually impossible to know, I gather—which would explain why I’ve never seen so much a guess.)

Infection in Cats
In the infamous “University of Nebraska-Lincoln paper,” published in 2010, the authors report—correctly, according to their source—that “most feral cats (62 percent to 80 percent) tested positive for toxoplasmosis.” [1] Trouble is, testing positive—seroprevalence—is simply not a useful measure of their ability to infect other animals or people.

“Most cats only shed oocysts for about one week in their life” (Note: The Atlantic suggests a three-week duration, as noted below) and seroconvert afterward. [2] “Thus, it is a reasonable assumption that most seropositive cats have already shed oocysts.” [2] “Testing positive,” in this case, is nothing more than the detection of antibodies resulting from seroconversion. Furthermore, because “most seronegative cats shed millions of oocysts after exposure to T. gondii… seropositive cats are likely to be less of a public health risk than seronegative cats.” [3]

Environmental Contamination
Because Flegr’s work doesn’t involve environmental contamination, McAuliffe only touched on the subject (“the parasite is typically picked up from the soil by scavenging or grazing animals—notably rodents, pigs, and cattle…”). For many TNR opponents, however, this is a hot topic—as some have suggested a direct connection between the presence of domestic cats and toxo-related infections in other animals, primarily land and marine mammals. (See, for example, my post from May 17 of last year.)

As a recent paper reports, bluntly: “Cats are the definitive host: the disease only occurs when cats are present.” [4] In fact, this claim is contradicted by a number of studies:

High levels (75 percent) of congenital transmission of T. gondii, for example, in a “wild population of mice,” led UK researchers to conclude “that this phenomenon might be more widespread than previously thought.” [5] Infections in sheep also point to congenital transmission, which “may be more important than previously considered.” [6]

The “high incidence of T. gondii found, among others, in free-living ruminants suggests a possibility of other, so far unknown, paths of transmission of this protozoan.” [7] “Due to the fact that they are widespread, and tick-bites occur frequently both in humans and in animals, ticks might play an important role in toxoplasmosis transmission.” [7]

Of particular interest are studies in the Arctic, where the prevalence of T. gondii infection in arctic foxes, Svalbard reindeer, sibling voles, walruses, kittiwakes, barnacle geese, and glaucous gulls “indicates that infection by oocysts is not an important mode of transmission on Svalbard.” [8] “T. gondii most likely is brought to Svalbard by migratory birds that become infected in temperate agricultural areas in the winter. However, marine sources of infection may exist. The high seroprevalence of T. gondii in the arctic fox population on Svalbard may be due to: (1) infection from migratory bird species through predation; (2) vertical transmission; and (3) tissue cyst transmission within the Svalbard ecosystem through scavenging and cannibalism. Together, these transmission routes cause a surprisingly high seroprevalence of T. gondii in a top predator living in an ecosystem with very few cats.” [8] Researchers studying infection rates in polar bears concluded: “It would… be inconceivable to assume that the few cats would play a major role in the epidemiology of T. gondii in the vast high Arctic. This is apparently the case in East Greenland as well.” [9]

In the Spring 2011 issue of The Wildlife Professional’s special section, “The Impact of Free Ranging Cats,” the authors argue: “Based on proximity and sheer numbers, outdoor pet and feral domestic cats may be the most important source of T. gondii oocysts in near-shore marine waters. Mountain lions and bobcats rarely dwell near the ocean or in areas of high human population density, where sea otter infections are more common.” [10] What the fail to acknowledge is that the most common type of T. gondii found to be infecting sea otters is the Type X strain, [11] which has yet to be traced to domestic cats, [12] or that “dual infections of T. gondii and S. neurona were more frequently associated with mortality and protozoal encephalitis than single infections, indicating a role for polyparasitism in disease severity.” [13]

Now What?
So, what are we to make of all this?

Or, as McAuliffe poses the question: “Given all the nasty science swirling around this parasite, is it time for cat lovers to switch their allegiance to other animals?”

Even Flegr would advise against that. Indoor cats pose no threat, he says, because they don’t carry the parasite. As for outdoor cats, they shed the parasite for only three weeks of their life, typically when they’re young and have just begun hunting. During that brief period, Flegr simply recommends taking care to keep kitchen counters and tables wiped clean. (He practices what he preaches: he and his wife have two school-age children, and two outdoor cats that have free roam of their home.)

Certainly, there’s still plenty we don’t know about T. gondii. A May 2011 article in Scientific American, for example, concedes simply: “The exact link between T. gondii and psychiatric diseases is tantalizing but remains murky.” [14]

Most telling of all may be the reaction of the pharmaceutical industry. Or, lack of a reaction, to be more precise. “Until solid proof exists that Toxo is as dangerous as some scientists now fear,” observes McAuliffe, “pharmaceutical companies don’t have much incentive to develop anti-Toxo drugs.” And if Big Pharma doesn’t think there’s money to be made here, how worried should we really be?